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In  C. elegans , the transcription factor skinhead-1 (SKN-1), the ortholog of human NF-E2-related factor 2 (Nrf-2), plays important roles in oxidative stress defense and aging processes. It has been documented that the activity of SKN-1 is regulated by its phosphorylation modification. However, whether other posttranslational modifications of SKN-1 affect its function remains unclear to date. Here we report, for the first time, that SKN-1 is  O -GlcNAcylated at Ser470 and Thr493 by  O- GlcNActransferase OGT-1. By generating the double mutations of Ser470/Thr493 in the wild type and  skn-1(zu67 ) worms, respectively, we found that disruption of  O -GlcNAc modification on SKN-1 repressed the accumulation of SKN-1 in the intestinal nuclei, and decreased the activities of SKN-1 in modulating lifespan and oxidative stress resistance. Moreover, under oxidative stress, SKN-1 was highly  O -GlcNAcylated, resulting in the decrease of GSK-3-mediated phosphorylation at Ser483 adjacent to the  O -GlcNAcylated residues (Ser470 and Thr493). These data suggest that  O -GlcNAcylation of SKN-1 is crucial for regulating lifespan and oxidative stress resistance via the crosstalk with its phosphorylation in  C. elegans . These findings have important implications for studying the functions of  O -GlcNAcylation on Nrf-2 in human aging-related diseases.

O-GlcNAcylation of SKN-1 modulates the lifespan and oxidative stress resistance in Caenorhabditis elegans